來自Washington大學(xué)（UW）兒童醫(yī)院及地區(qū)醫(yī)療中心的科學(xué)家們通過一項(xiàng)新研究發(fā)現(xiàn),，在過敏性疾病——例如過敏性皮炎，也叫濕疹——和自體免疫疾病之間存在特殊的聯(lián)系,。這一研究結(jié)果發(fā)表在4月1日出版的刊物《自然－免疫學(xué)》（Nature Immunology）上,。
大約有75%左右的自體免疫疾病發(fā)生在女性身上，其中絕大部分是處于分娩期的女性,。這些疾病同時(shí)還會(huì)造成很大一部分的童年期慢性異常等,。自體免疫疾病會(huì)導(dǎo)致超過80種非常嚴(yán)重的慢性疾病，其中包括神經(jīng),、胃腸道,、內(nèi)分泌系統(tǒng)的異常，以及皮膚和其它結(jié)締組織,、眼睛,、血液、和血管疾病等,。在所有這些疾病中,，其內(nèi)部的發(fā)病機(jī)制都是一致的——我們身體的免疫系統(tǒng)（包括B細(xì)胞和T細(xì)胞）變得失去方向，從而攻擊那些本應(yīng)被保護(hù)的器官,。
研究主要負(fù)責(zé)人,，來自UW兒童醫(yī)院的免疫學(xué)主任David Rawlings博士表示：“我們的研究結(jié)果表明，過敏性疾病和炎癥或許會(huì)觸發(fā)自體免疫疾病,，因?yàn)檫@些疾病會(huì)放松對(duì)于新產(chǎn)生的活躍B細(xì)胞的控制,。而以上過程非常重要，這是由于很多的自體免疫疾病都是由這些B細(xì)胞產(chǎn)生的自活躍抗體引起的。”
目前UW的科學(xué)家們正在尋找對(duì)于B細(xì)胞的控制的這種放松究竟發(fā)生在哪里,。Rawlings最后說：“通過和UW的實(shí)驗(yàn)室合作,，我們也在尋找治療這些疾病的藥物。現(xiàn)在一種幫助保護(hù)腎臟免受自體免疫疾病侵害的藥物正在進(jìn)行動(dòng)物實(shí)驗(yàn),。”
原始出處：http://www.physorg.com/news94837786.html
部分英文原文：
Published online: 1 April 2007; | doi:10.1038/ni1452
Local increase in thymic stromal lymphopoietin induces systemic alterations in B cell development
Alexander Astrakhan1, Miyuki Omori2, 7, Thuc Nguyen3, 7, Shirly Becker-Herman4, 7, Masanori Iseki2, 7, Theingi Aye2, Kelly Hudkins5, James Dooley6, Andrew Farr1, 6, Charles E Alpers5, Steven F Ziegler1, 2 & David J Rawlings1, 4
1 Department of Immunology, University of Washington School of Medicine Seattle, Washington 98195, USA.
2 Benaroya Research Institute, Seattle, Washington 98195, USA.
3 Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA.
4 Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, USA.
5 Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195, USA.
6 Department of Biological Structure, University of Washington School of Medicine, Seattle, Washington 98195, USA.
7 These authors contributed equally to this work.
Correspondence should be addressed to David J Rawlings [email protected] or Steven F Ziegler [email protected]
Abstract
The cytokine thymic stromal lymphopoietin (TSLP) drives immature B cell development in vitro and may regulate T helper type 2 responses. Here we analyzed the involvement of TSLP in B cell development in vivo with a doxycycline-inducible, keratin 5–driven transgene encoding TSLP (K5-TSLP). K5-TSLP-transgenic mice given doxycycline showed an influx of immature B cells into the periphery, with population expansion of follicular mature B cells, near-complete loss of marginal zone and marginal zone precursor B cells, and 'preferential' population expansion of peritoneal B-1b B cells. These changes promoted cryoglobulin production and immune complex–mediated renal disease. Identical events occurred in mice without T cells, in alternative TSLP-transgenic models and in K5-TSLP-transgenic mice with undetectable systemic TSLP. These observations suggest that signals mediating localized TSLP expression may modulate systemic B cell development and promote humoral autoimmunity.
